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Acute Pancreatitis (According to American College of Gastroenterology 2013 guidelines)

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This Presentation focuses on definition, new classification, different scoring systems for severity, rationale for radiological signs and new management recommendations as per 2013 American College of Gastroenterology guidelines

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Acute Pancreatitis (According to American College of Gastroenterology 2013 guidelines)

  1. 1. Acute Pancreatitis [Acute inflammation of abdominal tiger] (According to American College of Gastroenterology 2013 guidelines) Jibran Mohsin Resident, Surgical Unit I SIMS/Services Hospital Lahore
  2. 2. Outline • Introduction • Epidemiology • Pathophysiology • Etiology • Clinical Presentation • Workup • Severity Scoring System • Treatment • Prognosis • Complications
  3. 3. PANCREATITIS Inflammation in pancreas associated with injury to exocrine parenchyma PANCREAS Stroma Parenchyma Exocrine Primary injury causing PANCREATITIS Endocrine Involved secondarily or as a complication PANCREAS Greek word with literal meaning ‘pan’ (all/whole) , ‘creas’ (flesh): sweatbread
  4. 4. CLINICAL CLASSIFICATION *Considered a phase of chronic pancreatitis ** resulting from fibrosis within pancreas
  5. 5. ACUTE PANCREATITIS • CLINICAL DEFINITION – An acute condition presenting with abdominal pain-usually associated with raised blood/urine pancreatic enzymes as a result of pancreatic inflammation • PATHOLOGICAL DEFINITION – Reversible* pancreatic parenchymal injury associated with inflammation ___________________________________________________________ *if underlying cause of pancreatitis is removed, heal without any impairment of function or morphologic loss of gland *Recurrent attacks with irreversible parenchymal injury leading to impairment of function and morphologic loss is chronic pancreatitis
  6. 6. CLASSIFICATION OF ACUTE PANCREATITIS Atlanta* criteria (1992) • Mild acute pancreatitis (80% cases) (Acute Interstitial/edematous pancreatitis) – Acute Absence of organ failure – Absence of local complications • Severe acute pancreatitis(20 % cases) (Acute Hemorrhagic Necrotizing (fulminant) pancreatitis) – Local complications +/- – Organ failure defined as • SBP < 90 mm Hg • PaO2 ≤ 60 mm Hg • GI bleed ≥ 500 ml/24 hrs • Cret ≥ 2 mg/dL after rehydration – Ranson score ≥ 3 or APACHE ≥ 8 Revised Atlanta criteria (2012) • Mild acute pancreatitis – Absence of organ failure – Absence of local complications • Moderately severe acute pancreatitis – Local complications +/- – Transient organ failure(<48 h) • Severe acute pancreatitis – Persistent organ failure**(>48 h) and/or death *defined as a score of 2 or more for one of these(CVS, Renal, Resp) organ systems using the modified Marshall scoring system
  7. 7. Modified Marshall Scoring System for organ failure
  8. 8. Two Distinct phases of Acute Pancreatitis Early Phase(within 1 week) • Characterized by SIRS +/- organ failure • Severity assessed by functional/clinical Severity Scoring System (Ranson/Galsgow etc) Late Phase (>1 week) • Characterized by local complication • Severity assessed by morphological scoring system(Balthazar Scoring) __________________________________________________________________________ *Early clinical and the later morphologic classifications do not necessarily overlap and do not necessarily correlate with one another
  9. 9. Epidemiology World wide incidence ranges between 5 and 80 per 100,000 population GEOGRAPHICAL Highest incidence(worldwide) recorded in the United States and Finland(73.4 cases per 100,000)
  10. 10. Epidemiology Median ages of onset for various etiologies Etiology Median Ages of onset Alcohol-related 39 years Biliary tract–related 69 years Trauma-related 66 years Drug-induced etiology 42 years ERCP-related 58 years AIDS-related 31 years Vasculitis-related 36 years
  11. 11. Epidemiology Gender Predilection Generally M>F In males more often related to alcohol In females more often related to biliary tract disease Idiopathic pancreatitis no clear gender predilection AGE Young males and Old Females
  12. 12. Epidemiology RACE Hospitalization rates3 times higher for blacks than whites (racial differences more pronounced for males than females) Risk for African Americans aged 35-64 years10 times higher than for any other group
  13. 13. PATHOPHYSIOLOGY Autodigestion of pancreatic substance by inappropriately activated pancreatic enzymes (especially trypsinogen)
  14. 14. PATHOPHYSIOLOGY TRYPSINOGEN  TRYPSIN (hydrolysis of N- terminus hexapeptide by brush border enterokinase) Activation of prekallikrein Activation of kinin system Activation of Hageman factor-XII Activation of clotting and complement systems thrombosis and inflammation Activation of Phospholipase Activation of Prostaglandins and Bradykinins Lipase activation Triglycerides Glycerol + Fatty acids Fatty acids+ calcium saponified fat Hypocalcemia Elastase activation Digestion of elastic fibers Capillary leak/rupture/ Pseudoaneurysm 3rd space Sequestration of blood/fluid Hemorrhage+ Hypovolemic shock Activation of Lysolecithinase (derived from bile) Membrane damage Necrosis Release of inflammatory mediators into circulation systemic complications
  15. 15. MICROBIOLOGY-in infected necrosis • Commonly polymicrobial infection-60% • Source: – gall bladder, colon, small bowel(Transmural) or hematogenous spread • INCIDENCE: – 24%(1 week) and 70 %( 3 weeks) • ORGANISMS: – E.Coli(35%), klebsiella( 25%), Enterococcus (25%) – Others….. Staphlyococci, pseudomonas, proteus, enterobacter, anaerobes, candida(10%)
  16. 16. ACUTEPANCREATITIS Drinks like FISH (Dehydration) Burrows like RODENT (produces fistula) Stings like SCORPION (severe pain) Kills like LEOPARD (Life threatening) Eats like WOLF (Pancreatic Necrosis)
  17. 17. Etiology • Mechanical causes • Metabolic causes • Infective causes • Genetic causes • Vascular causes • Idiopathic AP
  18. 18. MECHANICAL CAUSES OF ACUTE PANCREATITIS Gall stones  Choledocholithiasis(40-70 %) • Most common biliary tract disease leading to AP • MOA: Ductal obstruction causing ductal hypertension and acinar cell injury • “Common channel hypothesis”-Opie in 1901(bile/activated enzymes reflux)- CONTROVERSIAL • Risk factors: inverse relation to size, wide cystic duct • 5 % of gall stones causes pancreatitis • M:F=1:3 Ampullary tumor sphincter of Oddi dysfunction Pancreatic CA(1-2 % ) • 5 % present as AP Choledochoceles, biliary sludge Abdominal trauma(1.5 %cases) • 17 % cases have high enzymes and 5 % have clinical AP • Penetrating>Blunt Iatrogenic Injury • Operative injury - Endoscopic procedures with dye injection
  19. 19. METABOLIC CAUSES OF ACUTE PANCREATITIS Alcoholism (25-35 %) • M:F=6:1 Hyperlipoproteinemia (1-4 %) • Type I and V hyperlipidemia • >1000 mg/dL(diagnostic criteria) • More severe than alcohol/gallstone Malnutrition Diabetes, Azotemia Porphyria Hypercalcemia/hyperparathyroidism • Hyper secretion and formation of calcified stones intraductallyAcinar injury Drugs (2 % cases)(usually mild) Definite association ( azathioprine, sulfonamaides, sulindac, tetracycline, valproic acid, Didanosine, Methyldopa,estrogens, furosemide, 6-Mercaptopurine, pentamidine, 5-ASA, steriods,octreotide) Probable association (thiazides, Flagyl, Methandienone, Nitrofurantoin, phenformin,piroxicam,procainamide, Colaspase, chlorthalidone, asparagine,cimetidine,cisplatin, cytosine arabinoside, diphenoxylate, ethacrynic acid)
  20. 20. INFECTIVE CAUSES OF ACUTE PANCREATITIS Viruses • MMR, Dengue virus(complication of dengue hemorrhagic fever MOA: Capillary leak3rd space loss), Coxsackie B, Hepatitis virus, CMV, EBV, Echovirus, VZV, HSV Bacteria • M. tuberculosis, M. avium complex, Mycoplasma, Legionella, Leptospira, Salmonella, Campylobacter, Yersinia, Brucella, Nocarbia Fungi • Aspergillus Parasites • Clonorchis sinensis, Toxoplasma, Cryptosporidium, Ascaris, Echinococcus granulosus, • Fasciola Hepatica, Opistorhcis sp and Dicrocoelium dendriticym Scorpion and snake bite • Trinidalian scorpion* (Tityus trinitatis) • MOA: Neurotransmitter discharge from cholinergic nerve terminals, leading to massive production of pancreatic juice(same MOA in antiacetylcholinesterase/OPC insecticide) *Most common cause of AP in Republic of Trinidad and Tobago, a twin island country off the northern edge of South America
  21. 21. GENETIC CAUSES OF AUTE PANCREATITIS Pancreas divisum (unfused ducts of Wirsung and Santorini) • Seen in 20-45 % cases • MOA(controversial): stenotic minor papillae and atretic duct of santorini Anomalous union of pancreaticobiliary duct(annular pancreas) Autoimmune pancreatitis-associated with IBD Hereditary pancreatitis- • Autosomal dominant, gain of function, mutations in cationic trypsinogen(PRSS1)with 80 % penetrance premature activation of trypsinogen • Mutation in trypsin inhibitor (SPINK1) genes blockade of active binding of trypsin rendering it inactive • Acute pancreatitis in teens • Chronic in next 2 decades • 40 % risk of pancreatic cancer by 70 year Celiac disease Cystic fibrosis-CFTR mutation  abnormality of ductal secretion
  22. 22. VASCULAR CAUSES OF ACUTE PANCREATITIS Shock Hypothermia Atheroembolism Vasculitis(Polyarteritis nodosa, SLE)
  23. 23. How Alcohol  Acute Pancreatitis??  Effects of diet  Malnutrition  Direct toxicity of alcohol  Concomitant tobacco smoking  Hypersecretion of gastric and pancreatic juices(rich in protein, low in bicarbonate/ trypsin inhibitor)protein plugsduct obstruction/reflux  Hyperlipidemia  Increased ductal permeability enzymes extrusion damage  Release of free radicals- superoxide, hydroxyl  Spasm of sphincter of Oddi
  24. 24. Alcohol-induced Pancreatitis • Manifests as a spectrum, ranging from discrete episodes of AP to chronic irreversible silent changes. • Diagnosis should not be entertained unless a person has a history of over 5-(15) years of heavy(>50 g per day, types less significant) alcohol consumption. • Clinically evident AP occurs in <5 % of heavy drinkers; thus, there are likely other factors that sensitize individuals to the effects of alcohol, such as genetic factors and tobacco use. • 1st attack is considered alcohol induced AP – Although it may be 1st manifestation of (acute on) chronic pancreatitis
  25. 25. Idiopathic Acute Pancreatitis • Defined as pancreatitis with no etiology established after initial laboratory (including lipid and calcium level,autoimmune markers, viral titers) and imaging tests (USG and CT in the appropriate patient) – In some patients an etiology may eventually be found(70 % of IAP due to microlithiasis), yet in others no definite cause is ever established. • Patients with IAP should be evaluated at centers of excellence focusing on pancreatic disease, providing advanced endoscopy services and a combined multidisciplinary approach. ________________________________________________________ Careful search for the etiology must be made in all cases, and no more than 20 % of cases should fall into the idiopathic category
  26. 26. Hyperlipidemia induced AP • In the absence of gallstones and/or history of significant history of alcohol use, a serum triglyceride should be obtained and considered the etiology if > 1,000 mg /d l • Lactescent (milky) serum has been observed in as many as 20 % of patients with AP • Therefore a fasting triglyceride level should be re-evaluated 1 month after discharge when hypertriglyceridemia is suspected • MOA: Lipase liberate large amounts of toxic fatty acids into pancreatic microcirculation • Leading to endothelial injury, sludging of blood cells, and consequent ischemic states
  27. 27. Iatrogenic-Operative Pancreatitis • Surgeries performed on/close to pancreas – Pancreatic biopsy – Biliary duct exploration – Distal or Billroth II gastrectomy – Jejunostomy – Splenectomy • Surgeries that use low systemic perfusion – Cardiopulmonary bypass (also due to hypothermia, atheromatous emboli) – Cardiac transplantation
  28. 28. Post-ERCP Pancreatitis • 3rd Most common cause of AP(after gallstone and alcohol) i.e. 4% • Most common complication of ERCP • INCIDENCE – 2-4 % (Historically, 5-10%) patients undergoing ERCP develop acute pancreatitis – Risk of severe AP < 1/500. • CAUSE – Duct disruption , enzyme extravasation • PREDISPOSING FACTORS – Sphincter of Oddi dysfunction(risk increases to 30 %) – H/O recurrent pancreatitis – Sphincterotomy – Balloon dilation of sphincter – Inexperienced endoscopist
  29. 29. CLINICAL MANIFESTATION
  30. 30. ABDOMEN PAIN-Cardinal Symptom • SITE: usually experienced first in the epigastrium – but may be localized to either upper quadrant or felt diffusely throughout the abdomen or lower chest • ONSET: characteristically develops quickly, generally following substantial meal and precedes NV • SEVERITY: frequently severe, reaching max. intensity within minutes rather than hours • NATURE: “boring through”, “knifing” (illimitable agony) • DURATION: hours-days • COURSE: constant (refractory to usual doses of analgesics, not relieved by vomiting) • RADIATION: directly to back(50%), chest or flanks • RELEIVING FACTOR: sitting or leaning/stooping forward (MUHAMMEDAN PRAYER SIGN) – due to shifting forward of abdominal contents and taking pressure off from inflamed pancreas • AGGRAVATING FACTOR: food/alcohol intake, walking, lying supine _______________________________________________________________________________ Pain described as dull, colicky, or located in the lower abdominal region is not consistent with AP and suggests an alternative etiology
  31. 31. OTHER MANIFESTATIONS • Nausea, frequent and effortless vomiting, anorexia,diarrhea – Due to reflex pylorospasm – More intense in necrotizing than in edematous pancreatitis • Persistent retching – despite empty stomach • Hiccups – Due to gastric distension/diaphragmatic irritation • Fever – Low grade, seen in infective pancreatitis • Weakness, Anxiety, Sweating – Indicates severe attack • Polyarthritis
  32. 32. General Physical Examination • Appearance: well  gravely ill with profound shock, toxicity and confusion • Vitals: Tachypnea(and dyspnea-10%), Tachycardia(65%), Hypotension, temp  high(76%)/normal/low (acute swinging pyrexia in cholangitis) • Icterus(28%) – gallstone pancreatitis or due to edema of pancreatic head • Cyanosis – Improper lung perfusion • Pallor, cold clammy skin,diaphoretic
  33. 33. ABDOMEN EXAMINATION • Tenderness + Rebound tenderness: – epigastrium/upper abdomen • Distension: – Ileus(BS decreased or absent) – ascites with shifting dullness • Mass in epigastrium(usually absent) – due to inflammation • Guarding(also called “defense musculaire” )-upper abdomen – tensing of the abdominal wall muscles to guard inflamed organs within the abdomen from the pain of pressure upon them(i.e. during palpation) • Rigidity(involuntary stiffness)-unusual – Tensing of the abdominal wall muscles to guard inflamed organs even if patient not touched
  34. 34. Cutaneous Ecchymosis(1 % cases)* Acute Hemorrhagic Necrotizing/fulminant Pancreatitis Periperitoneal/retroperitoneal Hemorrhage Methemalbumin formed from digested blood tracks around Fascial planes  hemorrhagic spots and ecchymosis in flanks (GREY TURNER’S SIGN)** FALCIFORM LIGAMENT  Bluish Discoloration around umbilicus (CULLEN’S SIGN) (umbllical black eye) Below inguinal ligament (FOX SIGN) *Neither sign is pathognomonic of acute pancreatitis *takes 24-48 hours to develop with 10-40 % mortality **More commonly, ruddy erythema in flanks due to extravasated pancreatic exudate
  35. 35. Differential Diagnosis GREY TURNER/CULLEN/FOX SIGNs • Acute Pancreatitis • Pancreatic Hemorrhage • Ruptured AAA • Blunt abdominal trauma • Ruptured ectopic pregnancy • Retroperitoneal hemorrhage • Coagulopathy Above: George Grey Turner Above: Thomas Stephen Cullen
  36. 36. GREY TURNER1 SIGN CULLEN2 SIGN FOX3 SIGN 1. Named after British surgeon George Grey Turner(1877-1951) 2. Named for Thomas Stephen Cullen (1869-1953), Canadian gynecologist who first described the sign in ruptured ectopic pregnancy in 1916 3.Named after George Henry Fox(1846-1937), American dermatologist
  37. 37. RESPIRATORY EXAMINATION Left sided* Pleural effusion(10-20%) + pulmonary edema+ pneumonitis Reduced chest movements+ decreased vocal fremitus/resonance + stony dull percussion note+ decreased air entry basally bilaterally + basal fine mid/end-inspiratory crepitation's- don’t change with cough *Due to close approximation of body and tail of pancreas to the left sided diaphragm
  38. 38. Neurological Examination Mild Psychosis Coma Toxemia Fat Embolism Hypoxia Respiratory distress Uremic encephlopathy Hypovolemic shock DIC
  39. 39. Other Manifestations • Subcutaneous fat necrosis – Small(<1 cm), red, tender nodules on extensor skin of legs • Purtscher retinopathy(on fundoscopy) – Activation of complement and agglutination of blood cells within retinal vessels causing Ischemic injury of retina – May cause temporary or permanent blindness
  40. 40. MANIFESTAIONS OF COMPLICATIONS • Hypocalcaemia – circumoral numbness or paresthesia (1st symtpom to develop) /tingling of distal extremities – carpopedal spasm (=main d'accoucheur- French "hand of the obstetrician”) • Flexion of wrist and MCP joints with extension of IP joints – laryngospasm – generalized seizures – Chvostek*(-Weiss) sign • Depending on calcium level, graded response occur: twitching first at angle of mouth, then by nose, the eye and the facial muscles • Positive in 10 % population in absence of hypocalcaemia – Trousseau** sign of latent tetany • BP cuff around arm and inflating to 20 mmHg above SBP for 3-5 minutes • Carpal spasm observed • More specific and sensitive than chvostek sign(postive even before tetany/hyperreflxia) *František Chvostek (German: Franz Chvostek) Czech-Austrian military physician (1835 – 1884), described this sign in 1876. **Armand Trousseau, French physican (1801-1867) described this phenomenon in 1861
  41. 41. MANIFESTAIONS OF COMPLICATIONS Hematemesis/ melena (5%) DIC Peripancreatic (duodenal) necrosis Gastric erosions
  42. 42. DIFFERENTIAL DIAGNOSIS ABDOMINAL CONDITONS • Perforated peptic ulcer/gastroentritis • Biliary colic/acute cholecystitis/ Cholangitis • Mesentric Ischemia • Ruptured Aortic Anuerysm • Intestinal Obstruction • Gastric/colon/pancreatic CA • Viral Hepatitis • IBS SYSTEMIC CONDITIONS • DKA THORAX CONDITIONS • Pneumonia/ARDS • Pleuritic pain • MI GYNECOLOGICAL CONDITONS • Ectopic pregnancy • Salpingtis
  43. 43. Diagnostic criteria • Most often established by the presence of two of the three following criteria: – (i) abdominal pain consistent with the disease, – (ii) serum amylase and/or lipase greater than three times the upper limit of normal, and/or – (iii) characteristic findings from abdominal imaging. _________________________________________________________ CT and/or MRI of the pancreas should be reserved for patients – in whom the diagnosis is unclear(typical pain with normal enzymes) – who fail to improve clinically within the first 48–72 h after hospital admission (e.g., persistent pain, fever, nausea, unable to begin oral feeding) – to evaluate complications
  44. 44. WORKUP • HEMATOLOGICAL investigations • RADIOLOGICAL investigations • Miscellaneous investigations
  45. 45. HEMATOLOGICAL • BASELINES – CBC: • Low Hb: prolonged hemetemesis/melena, internal hemorrhage • Leucocytosis (10,000-30,000/mcL)-infection, non infectious inflammation • Low platelets-DIC • Hct –raised in hemoconcentration – LFT’s: • raised bilirubin, AST/ALT/LDH, ALP, GGTP- gall stone pancreatitis – RFT’s: • raised BUN/cretainine- ATN ARF – Coagulation profile: • increased INR-DIC – BSR: • > 180 mg/dl-diabetes as a sequelae or cause – Serum electrolytes: • Low sodium/potassium: persistent vomiting • Hypocalcemia- saponification/fat necrosis – Serum Protein: • low protein/ albumin Diabetes Mellitus AP
  46. 46. HEMATOLOGICAL • ABG’s • Etiology specific investigations – Serum fasting lipid profile – Viral titers – Serum Calcium (HypercalcemiaAPHypocalcemia) – Autoimmune markers • increased serum levels of IgG4 • serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF), Acid-Base Disturbance Etiology Metabolic (Lactic)acidosis with high anion gap Hypovolemic shock Cholride-responsive Hypokalemic Hypochloremic metabolic alkalosis (Urine chloride < 20 mEq/L) persistent vomiting Respiratory acidosis ARDS/resp failure
  47. 47. HEMATOLOGICAL • Pancreatic Enzymes’ Assays – Serum Amylase: • ONSET: almost immediately • PEAK: within several hours – 3-4 times upper limit of normal within 24 hrs (90%) • RETURN to normal depends on severity(3-5 days) • normal at time of admission in 20% cases • Compared with lipase, returns more quickly to values below the upper limit of normal. – Serum Lipase: • more sensitive/specific than amylase • Remains elevated longer than amylase(12 days) • Useful if late presentation Raised Amylase  may not AP Normal Amylase  may be AP SERUM INDICATOR OF HIGHEST PROBABILITY OF DISEASE
  48. 48. • Pancreatic Enzymes’ Assays – Urine Amylase • More sensitive than serum levels • Remain elevated for several days after serum levels returned to normal – Pancreatic-specific amylase(p-amylase) • Measuring p-amylase instead to total amylase(also includes salivary amylase) makes diagnosis more specific(88-93%)
  49. 49. CONDITIONS ASSOCIATED WITH RAISED SERUM AMYLASE ABDOMEN • Small bowel obstruction – strangulation ileus – mesenteric ischemia • Acute appendicitis • Cholecystitis • Perforated Duodenal Ulcer • Gastroenteritis • Biliary peritonitis • Spasm of sphincter of Oddi GYNE • Ruptured Ectopic pregnancy • Torsion of an ovarian cyst OTHERS • Parotitis (Mumps) • Macroamylasaemia • Opioids administration • Low GFR • Brain injury(CVA)- hyperstimulation of pancreas
  50. 50. Plain CXR-PA view • Left sided Pleural effusion: blunting of costophrenic and cardiophrenic angles + haziness in lower zones • Elevated diaphragm on left side • Linear focal atelactasis of lower lobe of lungs • ARDS: diffuse alveolar interstitial shadowing • Pulmonary edema: prominent vascular markings _________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
  51. 51. Plain X-ray abdomen erect AP view • Sentinel* loop sign – Localized isolated Distended gut loop (Ileus) seen near the site of injured viscus or inflamed organ – RATIONALE: body's effort to localize the traumatic or inflamed lesions – ETIOLOGY: Localized paralysis followed by accumulation of gas – SITE: • Acute Pancreatitis Left hypochondrium (PROXIMAL JEJUNUM) • Acute Appendicitis Right iliac fossa • Acute Cholecystitis Right Hypochondrium • Diverticulitis Left iliac fossa *SENTINEL:A soldier stationed as a guard to challenge all comers and prevent a surprise attack _______________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
  52. 52. SENTINEL LOOP SIGN
  53. 53. Plain X-ray abdomen erect AP view • Colon cut-off sign – Gas filled (Distended) segment of proximal(mainly transverse) colon associated with narrowing of the splenic flexure – abruptly ending at the area of pancreatic inflammation – with collapse of descending colon – RANTIONALE: Extension of inflammatory process from the pancreas into the phrenicocolic ligament via the transverse mesocolon • resulting in functional spasm and/or mechanical narrowing of the splenic flexure at the level where the colon returns to the retroperitoneum. – Differential DIAGNOSIS: • IBD • Carcinoma of colon • Mesenteric Ischemia ____________________________________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
  54. 54. COLON CUT-OFF SIGN
  55. 55. Plain X-ray abdomen erect AP view • Renal halo sign – RATIONALE: peripancreatic inflammatory reaction extension into pararenal space – ETIOLOGY: water-density (radiolucent-halo)of inflammation in anterior pararenal space contrasts with perirenal fat; more common on left side • OTHERS _______________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis • Air in the duodenal C-loop • increased gastrocolic separation • Gastric curvature distortion • To rule out perforated DU(gas under diaphragm) • Obliteration of psoas shadow • Localized ground glass appearance ( localized increased high soft tissue density) • Calcified gall stones • Pancreatic calcification(chronic pancreatitis)
  56. 56. Renal Halo Sign NORMAL RENAL HALO SIGN
  57. 57. Transcutaneous Abdominal Ultrasonography • Not diagnostic • Should be performed within 24 hours in all patients to – detect gall stones* as a potential cause – Rule out acute cholecystits as differential diagnosis – Detect dilated CBD – sensitivity-(70-80%) – DEMERIT: overlying gas shadows 2ndary to bowel distension • THERAPEUTIC: – USG-guided aspiration for gram staining and culture – USG-guided pig tail catheter insertion ______________________________________________________________________________ * Identification of gallstones as the etiology should prompt referral for cholecystectomy to prevent recurrent attacks and potential biliary sepsis. Gallstone pancreatitis is usually an acute event and resolves when the stone is removed or passes spontaneously.
  58. 58. IV Contrast enhanced Computed Tomography Scan • Provides over 90 % sensitivity and specificity for the diagnosis of AP….. BUT • Routine use in patients with AP is unwarranted, as the diagnosis is apparent in many patients and most have a mild, uncomplicated course.
  59. 59. IV Contrast enhanced Computed Tomography Scan* • INDICATIONS-DIAGNOSTIC – Diagnostic uncertainty (differentiating pancreatitis from other possible intra- abdominal catastrophes) – Severe acute pancreatitis- distinguish interstitial from necrotizing pancreatitis • Necrosis( non enhancement area > 30 % or 3 cm) done at 72 hrs* – Systemic complications: • Progressive deterioration, MOF, sepsis – Localized complications: • Altered fat and fascial planes, Fluid collection, pseudocyst, psduoaneurysm, • Bowel distension, mesenteric edema, hemorrhage _____________________________________________________________ *INVESTIGATION OF CHOICE **Seldom needed within first 72 hrs after symptom onset unless the diagnosis is uncertain, because inflammatory changes are often not radiological present until this time
  60. 60. IV Contrast* enhanced Computed Tomography Scan • INDICATIONS-DIAGNOSTIC – Initial assessment of prognosis(CT severity index) – Perfusion CT at 3rd day  area of ischemia predict pancreatic necrosis • INDICATIONS-THERAPEUTIC: – CT-guided aspiration of fluid collection/necrotic tissue for gram staining and culture(sterile vs infected necrosis) – specimen should be delivered to the laboratory within an hour and interpreted promptly – CT-guided pig tail catheter insertion ______________________________________________________________ *Use of IV contrast may increase risk of complications of pancreatitis and AKI *Avoided if serum creatinine >1.5 mg/dL *MRI suitable alternative
  61. 61. BALTHAZAR CT severity index(CTSI)-1994 ___________________________________________________________________ Mild (0-3) moderate (4-6) severe (7-10) CT Severity Index Inflammation score + Necrosis score
  62. 62. Magnetic Resonant Imaging Suitable alternative to CT in patients with a contrast allergy and renal insufficiency where T2-weighted images without gadolinium contrast can diagnose pancreatic necrosis
  63. 63. Magnetic Resonant Cholangiopancreatography • INDICATION: – diagnosis of suspected biliary and pancreatic duct obstruction in the setting of pancreatitis. – Repeated attacks of idiopathic acute pancreatitis • Merit – used if choledocholithiasis is suspected but there is concern that pancreatitis might worsen is ERCP is performed – Provide non-invasive/fast/safe high-quality (Heavily T2– weighted) imaging for diagnostic and/or severity purposes
  64. 64. Endoscopic UltraSonography • INDICATIONS – Repeated idiopathic acute pancreatitis* • occult biliary disease- small stones/sludge • secretin-stimulated EUS study may reveal resistance to ductal outflow at the level of the papilla, – as evidenced by dilatation of the pancreatic duct to a greater extent and longer duration than in a healthy population – Age >40 to exclude malignancy • especially those with prolong or recurrent course • RATIONALE: 5 % CA pancreas present as AP _________________________________________ *Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, as the risks and benefits of investigation in these patients are unclear and should be referred to centers of expertise.
  65. 65. Endoscopic Retrograde Cholangiopancreatography INDICATION • Severe gallstone AP or AP with concurrent acute cholangitis/biliary obstruction/ biliary sepsis/jaundice (due to persistent stone) • ERCP within 24(-72) h of admission • Sphincterotomy/stent and bile duct clearance reduces infective complications/mortality NOT INDICATED • Not needed early in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction – As most of gallstones causing AP readily pass to duodenum and are lost in stool – MRCP or EUS recommended if CBD stone still suspected • as risk of post-ERCP pancreatitis is greater with normal calibre bile duct and normal bilirubin • MRCP /EUS as accurate as diagnostic ERCP
  66. 66. MISCELLANEOUS • Peritoneal(sensitivity 54%,specificity 93%)/Pleural fluid tap – High amylase/lipase/protein • Urine Complete Examination – Proteinuria, granular cast, glycosuria • Electrocardiography – ST-T wave changes • Bile Aspiration – Crystal analysis, if suspicion of microlithiasis • Manometry – Sphincterof Oddi dysfunction as a cause • Genetic testing – may be considered in young(<30 yrs) patients if no cause is evident and a family history (especially if >1 family member)of pancreatic disease is present
  67. 67. SEVERITY SCORING SYSTEMS ACUTE PANCREATITIS SPECIFIC SCORING SYSTEMS – Ranson score – Glagsow score – Bedside Index for Severity in Acute Pancreatitis(BISAP) score – Harmless Acute Pancreatitis Score(HAPS) – Hong Kong Criteria ACUTE PANCREATITIS NON-SPECIFIC SCORING SYSTEMS (ICU SCORING SYSTEMS) – Acute Physiology And Chronic Health Evaluation(APACHE) II score – Sequential Organ Failure Assessment(SOFA) score
  68. 68. Each system has merits and demerits, and none is currently recognized as a criterion standard ______________________________________
  69. 69. Although amylase/lipase are used in diagnosing pancreatitis, they are NOT use for predicting severity of disease _____________________________________ – i.e. patient with normal amylase(raised in 90 % cases) levels may still have severe acute pancreatitis
  70. 70. RANSON SCORE-1974 (for alcohol pancreatitis) ON ADMISSION • Age > 55 yrs • TLC > 16,000/mm3 • BSR> 200 mg/dL • AST > 250 IU/L • LDH > 350 IU/L WITHIN 48 HOURS • BUN rise >5 mg/dL • Pa02 < 60 mmHg ( 8 KPa) • Serum Calcium < 8 mg/dL • Base deficit > 4 meq/L • Fluid Sequestration > 6000 mL • Hct fall > 10 % NOTE: Disease classified as SEVERE when 3 or more factors are present
  71. 71. Revised RANSON SCORE-1979 (for Gallstone pancreatitis) ON ADMISSION • Age > 70 years • TLC > 18000/mm3 • BSR > 220 mg/dL • AST> 250 IU/L • LDH >400 IU/L WITHIN 48 HOURS • BUN rise >5 mg/dL • Pa02 < 60 mmHg ( 8 KPa) • Serum Calcium < 8 mg/dL • Base deficit > 5 meq/L • Fluid Sequestration > 4 litres • Hct fall > 10 % NOTE: Disease classified as SEVERE when 3 or more factors are present
  72. 72. RANSON SCORE Ranson score Mortality rate SEVERITY Interpretation 0-2 ≈ 0-2 % i.e. minimal mortality Mild AP Admit in regular ward 3-5 10-20 % Severe AP Admit in ICU/HDU 6-7 40 % Associated with more systemic complications >7 >50 % Same as above SCORING SYSTEM SENSITIVITY SPECIFICITY Ranson Criteria 73% 77% APACHE II 77% 84% CRP 73% 71%
  73. 73. RANSON SCORE……. DRAWBACKS • One has to measure all 11 signs to achieve the best predictability of prognosis • 2 full days are needed to complete the profile. – A delay of 48 hours after admission merely for assessment may squander a valuable opportunity to prevent a complication during this time. • Best used within the initial 48 hours of hospitalization and have not been validated for later time intervals. • Threshold for abnormal valve depends on whether cause is gallstone or alcohol • Only 73 % sensitive and 77 % specific in predicting mortality
  74. 74. Glasgow-Imrie score ON ADMISSION • Age > 55 yrs • TLC > 15 x 109 l-1 • BSR>180 mg/dL (10 mmol l-1) (no H/O diabetes) • BUN > 16 mmol l-1 (no response to IV fluids) • Pa02 < 60 mmHg ( 8 KPa) WITHIN 48 HOURS • Serum Calcium < 2.0 mmol l-1 • Serum albumin <32 g l-1 • LDH > 600 units l-1 • AST/ALT > 200 units l-1 NOTE: Disease classified as SEVERE when 3 or more factors are present
  75. 75. Modified Glasgow/PANCREAS score • PaO2 < 8kPa (60mmhg) • Age > 55 years • Neutrophils: WBC >15 x109/l • Calcium < 2mmol/l • Renal function: (Urea > 16mmol/l) • Enzymes: (AST/ALT > 200 iu/L or LDH > 600 iu/L) • Albumin < 32g/l • Sugar: (Glucose >10mmol/L) *Applicable for both gallstone and alcohol induced pancreatitis within 48 hours of admission *Omission of age/serum transaminase increases the predictive valve of scoring system as serum transaminase did not differ significantly between mild and severe pancreatitis *Bold 4 factors are independently significant in predicting the severity
  76. 76. Acute Physiology And Chronic Health Evaluation II score-1985 NOTE: Disease classified as SEVERE if clinical impression of very ill patient with APACHE II score above 8
  77. 77. APACHE Scoring System MERIT • Immediate assessment of the severity of pancreatitis possible • Can be used even after 48 hours • Unlike ALL pancreatic specific scoring systems, APACHE (and SOFA) also includes clinical features of patient besides laboratory values (Clinical findings are more important than lab findings in predicting SIRS,sepsis and other complications) • Best validated(medscape)
  78. 78. DEMERITS OF AP-specific scoring systems(ACG 2013) • Uniformly cumbersome, typically requiring 48 h to become accurate – when the score demonstrates severe disease, the patient’s condition is obvious regardless of the score. • Have a limited value, as they provide little additional information to the clinician in the evaluation of patients and may delay appropriate management. • No laboratory test is practically available or consistently accurate to predict severity in patients with AP. – Even the acute-phase reactant CRP, the most widely studied inflammatory marker in AP, is not practical as it takes 72 h to become accurate. – CT and/or MRI imaging also cannot reliably determine severity early in the course of AP, as necrosis usually is not present on admission and may develop after 24 – 48 h. _________________________________________________________________ Thus, in the absence of any available test to determine severity, close examination to assess early fluid losses, hypovolemic shock, and symptoms suggestive of organ dysfunction is crucial.
  79. 79. Predicting Severe AP(ACG 2013) So rather than depending on a scoring system to predict severity of AP, one need to be aware of intrinsic patient- related risk factors, including laboratory and imaging risk factors, for the development of severe disease.
  80. 80. Clinical findings associated with a severe course for initial risk assessment Patient characteristics Age > 55 years Obesity (BMI > 30 kg/m2) Altered mental status Comorbid disease SIRS (> 2 of the following criteria) pulse > 90 bpm Resp rate > 20/min or PaCO2 >4.3 KPa(32 mmHg) Temperature > 38 °C (100.4oF)or < 36 °C(96.8oF) TLC >12,000 or <4 ,000 cells/mm3 or > 10% immature neutrophils (bands) Laboratory findings BUN > 20 mg/dl Rising BUN Hct > 44% Rising Hct Elevated creatinine Radiology findings Pleural effusions Pulmonary infiltrates Multiple or extensive extrapancreatic collections
  81. 81. MANAGEMENT • Mild acute pancreatitis – Conservative Approach – Admit in general ward – Non invasive monitoring • (Moderate)Severe acute pancreatitis – Aggressive Approach – Admit in HDU/ICU – Invasive monitoring __________________________________________ Recognizing patients with severe acute pancreatitis ASAP is critical for achieving optimal outcomes
  82. 82. Mild Acute Pancreatitis • mild and self-limiting, needing only brief hospitalization. • Rehydration by IV fluids • Frequent non-invasive observation/monitoring(atleast 8 hrly) • Brief period of fasting till pain/vomiting settles – Little physiological justification for prolonged NPO • No medication required other than analgesics(important) and anti-emetics – Antibiotics not indicated in absence of signs or documented sources of infection – Pain results in ongoing cholinergic discharge, stimulating gastric and pancreatic secretions – Analgesics: WHO analgesic ladder-1986 – Avoid Morphine-cause sphincter of Oddi spasm • Metabolic support – Correction of electrolyte imbalance
  83. 83. Modified WHO analgesic Ladder
  84. 84. No or little role of……………….. • Nasogastric suction and H2-blockers • Secretion-inhibiting drugs – Atropine, calcitonin, somatostatin and its analogue(Octreotide) – glucagon and fluorouracil • Protease inhibiting drugs – Aprotinin, gabexate mesylate,camostate, phospholipase A2 inhibitors, FFP • Indomethacin or PG inhibitors • PAF antagonists – PAF acetylhydrolase, Lexipafant
  85. 85. Severe Acute Pancreatitis • P: – Pain relief – Proton pump inhibitors-omeprazole – Peritoneal lavage • A – Admit in HDU/ICU – Antibiotics • N – Nasogastric intubation(if vomiting) – Nasal oxygen – Nutrition support • C – Calcium gluconate – CVP line – Catherisation- Foley • R – Rehydration by IV fluids,plasma,blood – Ranitidine(for stress ulcer) – Radiology: CT scan, USG – Resuscitation when required • E – Endotracheal intubation – Electrolytes management – ERCP • A – Antacids • S – Swan-Ganz catheter for CVP and TPN – Suction-in case of aspiration – Steroids in case of ARDS – Supportive therapy for organ failure • Inotropes • Hemofiltration • Ventilator(PEEP)
  86. 86. Monitoring CLINICAL • Vitals • UOP • CV pressure INVESTIGATIONS • Baselines • Serial ABGs • Serial BSR • Serum calcium/magnesium
  87. 87. ACG 2013 Recommendations • Despite dozens of randomized trials, no medication has been shown to be effective in treating AP. • However, an effective intervention has been well described: EARLY AGRESSIVE IV hydration.
  88. 88. Rationale for EARLY AGRESSIVE IV hydration • Frequent hypovolemia due to – vomiting, – reduced oral intake, – third spacing of fluids(increased vascular permeability) – increased respiratory losses, and – diaphoresis. • Combination of microangiopathic effects and edema of the inflamed pancreas decreases blood flow, leading to increased cellular death, necrosis, and ongoing release of pancreatic enzymes activating numerous cascades. _________________________________________________________ *provides micro- and macrocirculatory support to prevent serious complications such as pancreatic necrosis
  89. 89. EARLY AGRESSIVE IV hydration Kon sa? Lactated Ringer ’s solution may be the preferred isotonic crystalloid replacement fluid • Ringer lactate is better electrolyte balance and more pH-balanced • Normal saline given in large volumes may lead to the development of a non-anion gap, hyperchloremic metabolic acidosis and increased chances of SIRS • Low pH activates the trypsinogen, makes the acinar cells more susceptible to injury and increases the severity of established AP Kab? Early aggressive IV hydration is most beneficial during the first 12 – 24 h, and may have little benefit beyond this time period Kitna? Aggressive hydration, defined as 250 – 500 ml per hour of isotonic crystalloid solution should be provided to all patients, unless cardiovascular, renal, or other related comorbid factors exist. • In a patient with severe volume depletion, manifest as hypotension and tachycardia, more rapid repletion (bolus) may be needed • Fluid requirements should be reassessed at frequent intervals within 6 h of admission and for the next 24 – 48 h.
  90. 90. EARLY AGRESSIVE IV hydration – Hematocrit and BUN has been widely recommended as surrogate markers for successful hydration • No absolute numbers recommended • Goal to decrease Hct and BUN and maintain normal cret – In elderly and cardiac/renal comorbidities hydration is monitored by • Central venous pressure via CV line or • Intrathoracic blood volume index – Better/more accurate correlate with cardiac index than CVP
  91. 91. Antibiotics • Routine use* NOT recommended(ACG 2013) as – Prophylaxis in severe AP – Preventive measure in sterile necrosis to prevent development of infected necrosis • Indicated in – Established infected pancreatic necrosis or – Extraperitoneal infections • Cholangitis, catheter-acquired infections, bacteremia, UTIs, pneumonia ______________________________________________ *Routine use of antifungal agents along with prophylactic or therapeutic antibiotics NOT recommended(ACG 2013)
  92. 92. Antibiotics • As SIRS may be indistinguishable from sepsis syndrome, so if infection is suspected, antibiotics should be given while source of infection is being investigated – Once blood and other cultures are found negative, antibiotics should be discontinued • Few antibiotics penetrate due to consistency of pancreatic necrosis – cefuroxime, or imipenem, or ciprofloxacin plus metronidazole
  93. 93. Antibiotics • Use of probiotics is associated with increased mortality in severe AP • Selective decontamination of bowel, targeting both bacteria and fungi, in order to prevent infected necrosis – Controversial • Relatively stable patients with infected necrosis can be managed conservatively on antibiotics without needing surgery(necrosectomy) or intervention (percutaneous or endoscopic drainage) – Surgical debridement recommended if no response to conservative treatment or deteriorates clinically
  94. 94. ……………………………………………………. Rather than preventing infection, the role of antibiotics in patients with necrotizing AP is NOW to treat established infected necrosis
  95. 95. Nutrition • In mild AP – oral feedings can be started immediately if there is no nausea/vomiting, and the abdominal pain/tenderness/Ileus has resolved(amylase return to normal, patient feel hunger) – Initiation of feeding with a small and slowly increasing low-fat (low-protein) soft diet appears as safe as a clear liquid diet, providing more calories • Stepwise manner increase from clear liquids to soft diet NOT necessary • In severe AP – Enteral route is recommended to prevent infectious complications – Parenteral nutrition should be avoided, unless enteral route is not available, not tolerated, or not meeting caloric requirements
  96. 96. RATIONALE OF EARLY ENTERAL NUTRITION • The need to place pancreas at rest until complete resolution of AP no longer seem imperative – Bowel rest associated with intestinal mucosal atrophy and bacterial translocation from gut and increased infectious complications • Early enteral feeding maintains the gut mucosal barrier, prevents disruption, and prevents translocation of bacteria that seed pancreatic necrosis – Decrease in infectious complications, organ failure and mortality
  97. 97. ……………………………………………….. Rather than using antibiotics to prevent infected necrosis………….start early enteral feeding to prevent translocation of bacteria RATIONALE MANAGEMENT PREVENTION OF STERILE NECROSIS Early aggressive IV hydration PREVENTION OF INFECTED NECCROSIS Early enteral feeding( NOT antibiotics) TREATMENT OF INFECTED NECROSIS Antibiotics, drainage, necrosectomy
  98. 98. Route of enteral Nutrition • Traditionally nasojejunal route has been preferred to avoid the gastric phase of stimulation BUT – Nasogastric route appears comparable in efficacy and safety MERITS OF NASOGASTRIC ROUTE DEMERITS OF NASOGASTRIC ROUTE NG tube placement is far easier than nasojejunal tube placement( requiring interventional radiology or endoscopy, thus expensive) especially in HDU/ICU setting Slight increased risk of aspiration (Can be overcome by placing patient in upright position and be placed on aspiration precautions)
  99. 99. Role of Surgery in AP • In case of mild gallstone AP, cholecystectomy should be performed before discharge to prevent a recurrence of AP – Within 48-72 hour od admission or briefly delay intervention(after 72 hrs but during same admission – Along with intraoperative cholangiography and any remaining CBD stones can be dealt with intra/post operative ERCP or – Along with preoperative EUS or MRCP • In case of necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be deferred until active inflammation subsides and fluid collections resolve or stabilize • Cholecysectomy done for recurrent AP (IAP) with no stones/sludge on USG and no significant elevation of LFTs is associated with >50 % recurrence of AP _________________________________________________________ If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone may be effective to reduce further attacks of AP
  100. 100. Sterile necrosis infected necrosis Asymptomatic doesnot mandate intervention regardless of size, location and extension surgical, radiologic, and/or endoscopic drainage should be delayed preferably for more than 4 weeks • to allow liquefaction of the contents and the development of a fibrous wall around the necrosis • Initially treated with antibiotics Stable Symptomatic (associated with GOO or bile obstruction) minimally invasive methods of necrosectomy are preferred to open necrosectomy Urgent debridement unstable Minimally invasive approach: laparoscopic surgery(ant or retroperitoneal approach), percutaneous radiologic catheter drainage or debridement, video-assisted or small incision- based left retroperitoneal debridement, and endoscopy
  101. 101. When to Discharge • Pain is well controlled with oral analgesia • Able to tolerate an oral diet that maintains their caloric needs, and • all complications have been addressed adequately Follow up • Routine clinical follow-up care (typically including physical examination and amylase and lipase assays) is needed to monitor for potential complications of the pancreatitis, especially pseudocysts. • Within 7-10 days
  102. 102. Recurrent AP CT scan •If neoplasia or chronic pancreatitis is found •addressed and treated accordingly. MRCP •shows developmental abnormalities, strictures, or evidence of chronic pancreatitis •endoscopic or surgical treatment may be of benefit in a subset of patients EUS •Microlithiasis/biliary sludge Cholecystectomy •Periammpullary mass missed on CT or MRCP Genetic •cationic trypsinogen mutations, SPINK1 mutations, or CFTR mutations ERCP •sphincter of Oddi manometry •Placed last because very high rate of post-ERCP pancreatitis(benefits< risk)
  103. 103. Prognosis TYPE OF AP MORTALITY Overall 10-15 % (Biliary>alcholic) Mild Acute Pancreatitis(80 % cases) 1 % Severe Acute Pancreatitis(20 % cases) Severe  20-50 % <1 week 1/3 cases MOF >1 week 2/3 cases Sepsis (+MOF)
  104. 104. SYSTEMIC COMPLICATIONS • CARDIOVASCULAR – Shock- hypovolemic and septic – Arrhythmias/pericardial effusion/sudden death – ST-T nonspecific changes • Pulmonary – Respiratory failure/pneumonia/atelectasis/pleural effusion – Acute Respiratory Distress Syndrome (ARDS) • Renal Failure – Oliguria – Azotemia – Renal artery/vein thrombosis • Hematological – Hemoconcentation – Disseminated Intravascular Coagulopathy (DIC)
  105. 105. SYSTEMIC COMPLICATIONS • Metabolic – Hypocalcemia – Hyperglycemia – Hyperlipidemia • Gastrointestinal – Peptic Ulcer/Erosive gastritis – Ileus – Portal vein or splenic vein thrombosis with varices • Neurological – Visual disturbances-Sudden blindness(Purtscher’s retinopathy) – Confusion,irritability,psychosis – Fat emboli – Alcohol withdrawal syndrome – Encephalopathy • Miscellaneous – Subcutaneous fat necrosis – Intra-abdominal saponification – Arthralgia
  106. 106. LOCAL COMPLICATIONS • Peripancreatic fluid collections • (Peri)Pancreatic necrosis( sterile + infected) • Pancreatic abscess(Phlegmon) • Pseudocyst • Pancreatic ascites • Pseudoaneurysm • Involvement of adjacent organs, with hemorrhage, thrombosis, bowel infraction, obstructive jaundice, fistula formation, or mechanical obstruction
  107. 107. THANK YOU……….

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